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Koma (tıp) Coma Koma hali Koma hali nedir? Hasta yakınlarının komadaki kişiyle görüşmesinin faydaları
Şeker koması Diabetic coma Yüksek şeker koması
Nonketotic hyperosmolar coma Hyperosmolar Hyperglycemic State Dehidratasyon
Hiperosmolar nonketotik diabet koması (enfeksiyon ve su açığıyla ortya çıkar, aşırı şeker yüklemede bitirir)
Komada su açığı dehidratasyon Kanda sodyum Keratin değerleri yükselir Osmolarity Ketotik Nonketotik diabet
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I Was Sinking Into a Diabetic Coma

I Was Sinking Into a Diabetic Coma

I Was Sinking Into a Diabetic Coma Hyperosmolar nonketotic diabetic coma


Hyperosmolar hyperglycemic state (HHS) is one of two serious metabolic derangements that occurs in patients with diabetes mellitus and can be a life-threatening emergency. The condition is characterized by hyperglycemia , hyperosmolarity , and dehydration without significant ketoacidosis. It is less common than the other acute complication of diabetes, diabetic ketoacidosis (DKA), and differs in the magnitude of dehydration, ketosis, and acidosis.

HHS usually presents in older patients with type 2 diabetes mellitus and carries a higher mortality rate than DKA, estimated at approximately 10-20%. (See Epidemiology.)

To see complete information on Diabetic Ketoacidosis, please go to the main article by clicking here.

Hyperosmolar hyperglycemic state most commonly occurs in patients with type 2 diabetes mellitus who have some concomitant illness that leads to reduced fluid intake. Infection is the most common preceding illness, but many other conditions can cause altered mentation, dehydration, or both. Once hyperosmolar hyperglycemic state has developed, it may be difficult to differentiate it from the antecedent illness. The concomitant illness may not be identifiable. (See Etiology.)

Most patients present with severe dehydration and focal or global neurologic deficits.[1, 2, 3] In as many as one third of cases, the clinical features of HHS and DKA overlap and are observed simultaneously (overlap cases). HHS was previously termed hyperosmolar hyperglycemic nonketotic coma (HHNC). However, the terminology was changed because coma is found in fewer than 20% of patients with HHS.[2] (See Clinical Presentation).

Based on the consensus statement published by the American Diabetic, diagnostic features of HHS may include the following (see Workup)[1, 4] :

Plasma glucose level of 600 mg/dL or greater Effective serum osmolality of 320 mOsm/kg or greater Profound dehydration up to an average of 9L Serum pH greater than 7.30 Bicarbonate concentration greater than 15 mEq/L Small ketonuria and absent-to-low ketonemia Some alteration in consciousness Detection and treatment of an underlying illness are critical. Standard care for dehydration and altered mental status is appropriate, including airway management, intravenous (IV) access, crystalloid, and any medications routinely given to coma patients. Although many patients with HHS respond to fluids alone, IV insulin in dosages similar to those used in DKA can facilitate correction of hyperglycemia. Insulin used without concomitant vigorous fluid replacement increases the risk of shock. (See Treatment and Management.)

To see complete information on Diabetes Mellitus, Type 1, please go to the main article by clicking here.

To see complete information on Diabetes Mellitus, Type 2, please go to the main article by clicking here.


In patients with a preexisting lack of or resistance to insulin, a physiologic stress such as an acute illness can cause further net reduction in circulating insulin. The basic underlying mechanism of hyperosmolar hyperglycemic state (HHS) is a reduction in the effective circulating insulin with a concomitant elevation of counter-regulatory hormones, such as glucagon, catecholamines, cortisol, and growth hormone.[1, 2]

Decreased renal clearance and decreased peripheral utilization of glucose lead to hyperglycemia. Hyperglycemia and hyperosmolarity result in an osmotic diuresis and an osmotic shift of fluid to the intravascular space, resulting in further intracellular dehydration. This diuresis also leads to loss of electrolytes, such as sodium and potassium.[1, 2, 3]

Unlike patients with diabetic ketoacidosis (DKA), patients with HHS do not develop significant ketoacidosis, but the reason for this is not known. Contributing factors likely include the availability of insulin in amounts sufficient to inhibit ketogenesis but not sufficient to prevent hyperglycemia. Additionally, hyperosmolarity itself may decrease lipolysis, limiting the amount of free fatty acids available for ketogenesis. Also, lower levels of counter-regulatory hormones have been found in patients with HHS compared with those with DKA.[1, 2, 3]


Hyperosmolar hyperglycemic state most commonly occurs in patients with type 2 diabetes mellitus who have some concomitant illness that leads to reduced fluid intake. In general, any illness that predisposes to dehydration may lead to HHS.[2, 3] A wide variety of major illnesses may trigger HHS by limiting patient mobility and free access to water.

A preceding or intercurrent infection is the most common cause, but the concomitant illness may not be identifiable. Pneumonia and urinary tract infections (UTIs) are the most common underlying causes of HHS.[2]

Stress response to any acute illness tends to increase hormones that favor elevated glucose levels. Cortisol, catecholamines, glucagon, and many other hormones have effects that tend to counter those of insulin. Examples of such acute conditions are as follows:

Stroke Intracranial hemorrhage Silent myocardial infarction Pulmonary Embolism Patients with underlying renal dysfunction and/or congestive heart failure are at greater risk.

Drugs that raise serum glucose levels, inhibit insulin, or cause dehydration may cause HHS. Examples include the following:

Diuretics Beta-blockers Atypical antipsychotics (clozapine, olanzapine) Alcohol and cocaine Total parenteral nutrition and fluids that contain dextrose Noncompliance with oral hypoglycemics or insulin therapy can result in HHS.

Elder abuse and neglect also may contribute to underhydration.


United States statistics The incidence of hyperosmolar hyperglycemic state is less than 1 case per 1000 person-years, making it significantly less common than diabetic ketoacidosis. As the prevalence of type 2 diabetes mellitus increases, the incidence of HHS will likely increase as well.[2]

Age and sex distribution for HHS HHS has a mean age of onset early in the seventh decade of life.[2, 3, 5] In contrast, the mean age for DKA is early in the fourth decade of life. Residents of nursing facilities who are elderly and demented are at the highest risk due to a lack of ability to care for themselves. The prevalence is slightly higher in females than in males.

HHS in children As rates of obesity increase in children, the prevalence of type 2 diabetes mellitus is also rising in this age group and may lead to an increased incidence of HHS in this population.[6, 7, 8]

Prevalence of HHS by race African Americans, Hispanics, and Native Americans are disproportionately affected due to an increased prevalence of type 2 diabetes mellitus.[2]


Overall mortality rate is between 10 and 20% and is usually due to a comorbid illness. The mortality rate of HHS increases with increasing age and with higher levels of serum osmolality.

The mortality due to HHS in children also appears to be higher as compared to DKA, but there have been too few reported cases to calculate mortality accurately.

Patient Education Diabetic teaching is necessary to prevent recurrence.

History Most patients with hyperosmolar hyperglycemic state (HHS) have a known history of diabetes, which is usually type 2. In 30-40% of cases, HHS is the patient’s initial presentation of diabetes.[3]

HHS usually develops over a course of days to weeks, unlike diabetic ketoacidosis (DKA), which develops more rapidly. Often, a preceding illness results in several days of increasing dehydration. Adequate oral hydration may be impaired by concurrent acute illness (eg, vomiting) or chronic comorbidity (eg, dementia, immobility).

Patients may complain of polydipsia, polyuria, weight loss, and weakness. They do not typically report abdominal pain, a complaint that is often noted in patients with DKA.

A wide variety of focal and global neurologic changes may be present, including the following:

Drowsiness and lethargy Delirium Coma Focal or generalized seizures Visual changes or disturbances Hemiparesis Sensory deficits Physical Examination Examine the patient for evidence of hyperosmolar hyperglycemic state (HHS), focusing on hydration status, mentation, and signs of possible underlying causes, such as a source of infection. General appearance and hygiene may provide clues to the state of hydration, presence of chronic illness, and reduced level of mentation. Hypoxemia can be a concurrent problem affecting mentation.

The extremities may manifest evidence of peripheral volume sequestration or of dehydration.

Vital signs Tachycardia is an early indicator of dehydration; hypotension is a later sign suggestive of profound dehydration due to volume loss secondary to osmotic diuresis. Tachypnea may occur due to respiratory compensation for metabolic acidosis in overlap cases.

Assess core temperature rectally. Abnormally high or low temperatures suggest sepsis as an underlying cause. Lack of fever does not rule out infection. Hypothermia is a poor prognostic factor.

Orthostatic vital signs are neither sensitive nor specific for volume status.

Skin examination Perform a thorough skin examination. Skin turgor is another clue to hydration status.

Head, eyes, ears, nose, and throat examination Examine the head, eyes, ears, nose, and throat. Examination may reveal altered hydration status (eg, sunken eyes, dry mouth). Cranial neuropathies, visual field losses, and nystagmus may be appreciated, which are symptoms of HHS. They are usually reversible with therapy.

Diagnostic ConsiderationsEdit

The differential diagnosis includes any cause of altered mental status, such as the following[2] :

Central nervous system infection Hypoglycemia Hyponatremia Severe dehydration Uremia Hyperammonemia Drug overdose Sepsis Differentials Approach Considerations Diabetic ketoacidosis is typically characterized by hyperglycemia over 300 mg/dL, a bicarbonate level less than 15 mEq/L, and a pH less than 7.30, with ketonemia and ketonuria.

While definitions vary, moderate DKA can be categorized by a pH less than 7.2 and a serum bicarbonate less than 10 mEq/L, whereas severe DKA has a pH less than 7.1 and bicarbonate less than 5 mEq/L.

Laboratory studies for diabetic ketoacidosis (DKA) should be scheduled as follows:

Blood tests for glucose every 1-2 h until patient is stable, then every 6 h Serum electrolyte determinations every 1-2 h until patient is stable, then every 4-6 h Initial blood urea nitrogen (BUN) Initial arterial blood gas (ABG) measurements, followed with bicarbonate as necessary Repeat laboratory tests are critical, including potassium, glucose, electrolytes, and, if necessary, phosphorus. Initial workup should include aggressive volume, glucose, and electrolyte management.

It is important to be aware that high serum glucose levels may lead to dilutional hyponatremia; high triglyceride levels may lead to factitious low glucose levels; and high levels of ketone bodies may lead to factitious elevation of creatinine levels.

Serum Glucose Study The blood glucose level for patients with DKA usually exceeds 250 mg/dL. The clinician can perform a fingerstick glucose test while waiting for the serum chemistry panel.

Urine Dipstick Testing For patients with DKA, the urine dipstick test is highly positive for glucose and ketones. Rarely, urine is negative for ketones, due to the fact that most available laboratory tests can detect only acetoacetate, while the predominant ketone in severe untreated DKA is beta-hydroxybutyrate.

When the clinical condition improves with treatment, the urine test result becomes positive due to the returning predominance of acetoacetate. To detect underlying urinary infection, look for glycosuria and urine ketosis.

Ketones In patients with DKA, serum ketones are present. Blood beta-hydroxybutyrate levels measured by a reagent strip (Ketostix, N-Multistix, and Labstix) and serum ketone levels assessed by the nitroprusside reaction are equally effective in diagnosing DKA in uncomplicated cases.

The Acetest and Ketostix products measure blood and urine acetone and acetoacetic acid. They do not measure the more common ketone body, beta-hydroxybutyrate, so the patient may have paradoxical worsening as the latter is converted into the former during treatment.

Specific testing for beta-hydroxybutyrate can be performed by many laboratories. Diagnosis of ketonuria requires adequate renal function. Additionally, ketonuria may last longer than the underlying tissue acidosis.

One study suggests that routine urine testing for ketones is no longer necessary to diagnose DKA.[11] Using capillary beta hydroxybutyrate offers a distinct advantage of avoiding unnecessary work-up.

According to the 2011 Joint British Diabetes Societies (JBDS) guideline for the management of diabetic ketoacidosis, capillary blood ketones should be measured in order to monitor the response to DKA treatment. The method of choice is bedside measurement of blood ketones using a ketone meter. In the absence of blood ketone measurement, venous pH and bicarbonate should be used together with bedside blood glucose monitoring to evaluate treatment response.[12, 13]

Beta-Hydroxybutyrate Serum or capillary beta-hydroxybutyrate can be used to follow response to treatment in patients with DKA. levels greater than 0.5 mmol/L are considered abnormal, and levels of 3 mmol/L correlate with the need for treatment for DKA.[14]

Arterial Blood Gases In patients with DKA, arterial blood gases (ABGs) frequently show typical manifestations of metabolic acidosis, low bicarbonate, and low pH (< 7.2).

When monitoring the response to treatment, the 2011 JBDS guideline recommends the use of venous blood rather than arterial blood in blood gas analyzers, except where respiratory problems preclude using arterial blood.[12, 13]

Venous pH may be used for repeat pH measurements.[15] Brandenburg and Dire found that pH on venous blood gas in patients with DKA was 0.03 lower than pH on ABG.[16] Because this difference is relatively reliable and not of clinical significance, there is almost no reason to perform the more painful ABG. End tidal CO2 has been reported as a way to assess acidosis as well.

Serum Electrolyte Panel Serum potassium levels initially are high or within the reference range in patients with DKA. This is due to the extracellular shift of potassium in exchange of hydrogen, which is accumulated in acidosis, in spite of severely depleted total body potassium. This needs to be checked frequently, as values drop very rapidly with treatment. An ECG may be used to assess the cardiac effects of extremes in potassium levels.

The serum sodium level usually is low in affected patients. The osmotic effect of hyperglycemia moves extravascular water to the intravascular space. For each 100 mg/dL of glucose over 100 mg/dL, the serum sodium level is lowered by approximately 1.6 mEq/L. When glucose levels fall, the serum sodium level rises by a corresponding amount.

Additionally, serum chloride levels and phosphorus levels always are low in these patients.

Bicarbonate Use bicarbonate levels in conjunction with the anion gap to assess the degree of acidosis that is present.

Anion Gap In patients with diabetic ketoacidosis, the anion gap is elevated ([Na + K] - [Cl + HCO3] >13 mEq/L).

CBC Count Even in the absence of infection, the CBC count shows an increased white blood cell (WBC) count in patients with diabetic ketoacidosis. High WBC counts (>15 X 109/L) or marked left shift may suggest underlying infection.

Renal Function Studies BUN frequently is increased in patients with diabetic ketoacidosis.

Osmolarity Plasma osmolarity usually is increased (>290 mOsm/L) in patients with diabetic ketoacidosis. If plasma osmolarity cannot be measured directly, it may be calculated with the following formula: plasma osmolarity = 2 (Na + K) + BUN/3 + glucose/18. Urine osmolarity also is increased in affected patients.

Patients with diabetic ketoacidosis who are in a coma typically have osmolalities greater than 330 mOsm/kg H2 O. If the osmolality is less than this in a patient who is comatose, search for another cause of obtundation.

Cultures Urine and blood culture findings help to identify any possible infecting organisms in patients with diabetic ketoacidosis.

Amylase Hyperamylasemia may be seen in patients with diabetic ketoacidosis, even in the absence of pancreatitis.

Phosphate, Calcium, and Magnesium If the patient is at risk for hypophosphatemia (eg, poor nutritional status, chronic alcoholism), then the serum phosphorous level should be determined.

Chest Radiography Chest radiography should be used to rule out pulmonary infection such as pneumonia.

MRI An MRI is helpful in detecting early cerebral edema; it should be ordered only if altered consciousness is present.[7]

CT Scanning The threshold should be low for obtaining a head CT scan in children with diabetic ketoacidosis who have altered mental status, as this may be caused by cerebral edema.

Many of the changes may be seen late on head imaging and should not delay administration of hypertonic saline or mannitol in those pediatric cases where cerebral edema is suspected.

Electrocardiography DKA may be precipitated by a cardiac event, and the physiological disturbances of DKA may cause cardiac complications. An ECG should be performed every 6 hours during the first day, unless the patient is monitored. An ECG may reveal signs of acute myocardial infarction that could be painless in patients with diabetes, particularly in those with autonomic neuropathy.

An ECG is also a rapid way to assess significant hypokalemia orhyperkalemia. T-wave changes may produce the first warning sign of disturbed serum potassium levels. Low T wave and apparent U wave always signify hypokalemia, while peaked T wave is observed in hyperkalemia.

Telemetry Consider telemetry in patients with comorbidities (especially cardiac), known significant electrolyte abnormalities, severe dehydration, or profound acidosis


Considerations Managing diabetic ketoacidosis (DKA) in an intensive care unit during the first 24-48 hours always is advisable. When treating patients with DKA, the following points must be considered and closely monitored:

Correction of fluid loss with intravenous fluids Correction of hyperglycemia with insulin Correction of electrolyte disturbances, particularly potassium loss Correction of acid-base balance Treatment of concurrent infection, if present It is essential to maintain extreme vigilance for any concomitant process, such as infection, cerebrovascular accident, myocardial infarction, sepsis, ordeep venous thrombosis.

It is important to pay close attention to the correction of fluid and electrolyte loss during the first hour of treatment. This always should be followed by gradual correction of hyperglycemia and acidosis. Correction of fluid loss makes the clinical picture clearer and may be sufficient to correct acidosis. The presence of even mild signs of dehydration indicates that at least 3 L of fluid has already been lost.

Patients usually are not discharged from the hospital unless they have been able to switch back to their daily insulin regimen without a recurrence of ketosis. When the condition is stable, pH exceeds 7.3, and bicarbonate is greater than 18 mEq/L, the patient is allowed to eat a meal preceded by a subcutaneous (SC) dose of regular insulin.

Insulin infusion can be discontinued 30 minutes later. If the patient is still nauseated and cannot eat, dextrose infusion should be continued and regular or ultra–short-acting insulin should be administered SC every 4 hours, according to blood glucose level, while trying to maintain blood glucose values at 100-180 mg/dL.

The 2011 JBDS guideline recommends the intravenous infusion of insulin at a weight-based fixed rate until ketosis has subsided. Should blood glucose fall below 14 mmol/L (250 mg/dL), 10% glucose should be added to allow for the continuation of fixed-rate insulin infusion.[12, 13]

In established patients with diabetes, SC long-acting insulin (eg, insulin glargine, Detemir, Ultralente) should be initiated at the dose that was used prior to the manifestation of DKA. If neutral protamine Hagedorn (NPH) insulin was used previously, however, start back at the usual dose only when the patient eats well and is able to retain meals without vomiting; otherwise, the dose should be reduced to avoid hypoglycemia during its peak efficacy period.

In newly diagnosed patients with type 1 diabetes, a careful estimate of the long-acting insulin dose should be considered. Starting with smaller doses generally is recommended to avoid hypoglycemia.

See Diabetes Mellitus, Type 1 and Diabetes Mellitus, Type 2 for more complete information on these topics.

Correction of Fluid Loss Fluid resuscitation is a critical part of treating patients with DKA. Intravenous solutions replace extravascular and intravascular fluids and electrolyte losses. They also dilute both the glucose level and the levels of circulating counterregulatory hormones. Insulin is needed to help switch from a catabolic state to an anabolic state, with uptake of glucose in tissues and the reduction of gluconeogenesis as well as free fatty acid and ketone production.

Initial correction of fluid loss is either by isotonic sodium chloride solution or by lactated Ringer solution. The recommended schedule for restoring fluids is as follows:

Administer 1-3 L during the first hour. Administer 1 L during the second hour. Administer 1 L during the following 2 hours Administer 1 L every 4 hours, depending on the degree of dehydration and central venous pressure readings When the patient becomes euvolemic, the physician may switch to half the isotonic sodium chloride solution, particularly if hypernatremia exists. Isotonic saline should be administered at a rate appropriate to maintain adequate blood pressure and pulse, urinary output, and mental status.

If a patient is severely dehydrated and significant fluid resuscitation is needed, switching to a balanced electrolyte solution (eg, Normosol-R, in which some of the chloride in isotonic saline is replaced with acetate) may help to avoid the development of a hyperchloremic acidosis.

When blood sugar decreases to less than 180 mg/dL, isotonic sodium chloride solution is replaced with 5-10% dextrose with half isotonic sodium chloride solution.

After initial stabilization with isotonic saline, switch to half-normal saline at 200-1000 mL/h (half-normal saline matches losses due to osmotic diuresis).

Insulin should be started about an hour after IV fluid replacement is started to allow for checking potassium levels and because insulin may be more dangerous and less effective before some fluid replacement has been obtained.

Although the incidence of life-threatening hypokalemia due to aggressive insulin administration is very low, there is little to no advantage in starting insulin prior to rehydration and evaluation of serum potassium levels. Initial bolus of insulin does not change overall management of DKA.[17]

Pediatric protocols to minimize the risk of cerebral edema by reducing the rate of fluid repletion vary. The International Society for Pediatric and Adolescent Diabetes (ISPAD) Clinical Practice Consensus Guidelines suggest initial fluid repletion in pediatric patients should be 10-20 mL/kg of normal saline (0.9%) solution during the first 1-2 hours without initial bolus, and then, after 1-2 hours, insulin should be started to avoid pediatric cerebral edema.[18]

ISPAD provides detailed fluid administration guidelines. Total volume over the first 4 hours should not exceed 40-50 mL/kg. Fluid administration is as vital in children as in adults.

Insulin Therapy When insulin treatment is started in patients with DKA, several points must be considered. A low-dose insulin regimen has the advantage of not inducing the severe hypoglycemia or hypokalemia that may be observed with a high-dose insulin regimen.

Only short-acting insulin is used for correction of hyperglycemia. Subcutaneous absorption of insulin is reduced in DKA because of dehydration; therefore, using intravenous or intramuscular routes is traditionally preferable.

SC use of the fast-acting insulin analog (lispro) has been tried in pediatric DKA (0.15 U/kg q2h). The results were shown to be comparable to IV insulin, but ketosis took 6 additional hours to resolve. Such technically simplified methods may be cost-effective and may preclude admissions to intensive care units in patients with mild cases.

The initial insulin dose is a continuous IV insulin infusion using an infusion pump, if available, at a rate of 0.1 U/kg/h. A mix of 24 units of regular insulin in 60 mL of isotonic sodium chloride solution usually is infused at a rate of 15 mL/h (6 U/h) until the blood glucose level drops to less than 180 mg/dL; the rate of infusion then decreases to 5-7.5 mL/h (2-3 U/h) until the ketoacidotic state abates.

Larger volumes of an insulin and isotonic sodium chloride solution mixture can be used, providing that the infusion dose of insulin is similar. Larger volumes may be easier in the absence of an IV infusion pump (eg, 60 U of insulin in 500 mL of isotonic sodium chloride solution at a rate of 50 mL/h).

The optimal rate of glucose decline is 100 mg/dL/h. Do not allow the blood glucose level to fall below 200 mg/dL during the first 4-5 hours of treatment. Hypoglycemia may develop rapidly with correction of ketoacidosis.

Allowing blood glucose to drop to hypoglycemic levels is a common mistake that usually results in a rebound ketosis derived by counter-regulatory hormones. Rebound ketosis necessitates a longer duration of treatment. The other hazard is that rapid correction of hyperglycemia and hyperosmolarity may shift water rapidly to the hyperosmolar intracellular space and may induce cerebral edema.

Although DKA was a common problem in patients with diabetes who were treated with continuous subcutaneous insulin infusion through insulin infusion pumps, the incidence of DKA was reduced with the introduction of pumps equipped with sensitive electronic alarm systems that alert users when the infusion catheter is blocked.

Electrolyte Correction If the potassium level is greater than 6 mEq/L, do not administer potassium supplement. If the potassium level is 4.5-6 mEq/L, administer 10 mEq/h of potassium chloride. If the potassium level is 3-4.5 mEq/L, administer 20 mEq/h of potassium chloride.

Monitor serum potassium levels hourly, and the infusion must be stopped if the potassium level is greater than 5 mEq/L. The monitoring of serum potassium must continue even after potassium infusion is stopped in the case of (expected) recurrence of hypokalemia.

In severe hypokalemia, not starting insulin therapy is advisable unless potassium replacement is under way; this is to avert potentially serious cardiac dysrhythmia that may result from hypokalemia.

Potassium replacement should be started with initial fluid replacement if potassium levels are normal or low. Add 20-40 mEq/L of potassium chloride to each liter of fluid once the potassium level is less than 5.5 mEq/L. Potassium can be given as follows: two thirds as KCl, one third as KPO4.

Correction of Acid-Base Balance Sodium bicarbonate only is infused if decompensated acidosis starts to threaten the patient's life, especially when associated with either sepsis or lactic acidosis. If sodium bicarbonate is indicated, 100-150 mL of 1.4% concentration is infused initially. This may be repeated every half hour if necessary. Rapid and early correction of acidosis with sodium bicarbonate may worsen hypokalemia and cause paradoxical cellular acidosis.

Bicarbonate typically is not replaced as acidosis will improve with the above treatments alone. Administration of bicarbonate has been correlated with cerebral edema in children.

Treatment of Concurrent Infection In the presence of infection, the administration of proper antibiotics is guided by the results of culture and sensitivity studies. Starting empiric antibiotics on suspicion of infection until culture results are available may be advisable.

See Diabetic Foot Infections and Diabetic Ulcers for more complete information on these topics.

Management of Treatment-Edit

Related Complications Cerebral edema Cerebral edema is a serious, major complication that may evolve at any time during treatment of DKA and primarily affects children. It is the leading cause of DKA mortality in children.

Be extremely cautious to avoid cerebral edema during initiation of therapy. Deterioration of the level of consciousness in spite of improved metabolic state usually indicates the occurrence of cerebral edema. MRI usually is used to confirm the diagnosis.

Cerebral edema that occurs at initiation of therapy tends to worsen during the course of treatment. Mannitol or hypertonic saline should be available if cerebral edema is suspected.

According to Wolfsdorf et al, 0.5-1 g/kg intravenous mannitol may be given over the course of 20 minutes and repeated if no response is seen in 30-120 minutes.[18] Also, if no response to mannitol occurs, hypertonic saline (3%) may be given at 5-10 mg/kg over the course of 30 minutes.

Clinical cerebral edema is rare and carries the highest mortality rate. Although mannitol (0.25-1 g/kg IV) and dexamethasone (2-4 mg q6-12h) frequently are used in this situation, no specific medication has proven useful in such instances.

Recent research by Glaser et al indicated that cerebral edema occurs in 1% of children with DKA, with a mortality rate of 21% and neurologic sequelae in another 21% of patients. Glaser et al suggested that up to half of children with DKA have subtle brain MRI findings, particularly with respect to narrowing of the lateral ventricles.[19]

Muir et al have identified diagnostic criteria for cerebral edema that include abnormal response to pain, decorticate and decerebrate posturing, cranial nerve palsies, abnormal central nervous system respiratory patterns, fluctuating level of consciousness, sustained heart rate deceleration, incontinence, and more nonspecific criteria such as vomiting, headache, lethargy, and elevated diastolic blood pressure.[20]

Cerebral edema begins with mental status changes and is believed to be due partially to idiogenic osmoles, which have stabilized brain cells from shrinking while the diabetic ketoacidosis was developing.

The risk of cerebral edema is related to the severity and duration of DKA. It is often associated with ongoing hyponatremia. Cerebral edema is correlated with the administration of bicarbonate. Concerns about the role of overaggressive or overly hypotonic fluid resuscitation as a cause of the edema that have been raised in the past correlate more closely with disease severity than with rapid administration of fluids.[21]

Cardiac dysrhythmia

Cardiac dysrhythmia may occur secondary to severe hypokalemia and/or acidosis either initially or as a result of therapy in patients with DKA. Usually, correction of the cause is sufficient to treat cardiac dysrhythmia, but if it persists, consultation with a cardiologist is mandatory. Performing cardiac monitoring on patients with DKA during correction of electrolytes always is advisable.

Pulmonary edema

Pulmonary edema may occur for the same reasons as cerebral edema in patients with diabetic ketoacidosis. Be cautious of possible overcorrection of fluid loss, though it occurs only rarely.

Although initial aggressive fluid replacement is necessary in all patients, particular care must be taken in those with comorbidities such as renal failureor congestive heart failure. Diuretics and oxygen therapy often suffice for the management of pulmonary edema.

Myocardial injury Nonspecific myocardial injury may occur in severe DKA, which is associated with minute elevations of myocardial biomarkers (troponin T and CK-MB) and initial ECG changes compatible with myocardial infarction (MI).

Acidosis and very high levels of free fatty acids could cause membrane instability and biomarker leakage. Coronary arteriography usually is normal, and patients tend to recover fully without further evidence of ischemic heart disease. Regardless of the pathogenesis, the presence of minute biomarker elevations and ECG changes do not necessarily signify MI in DKA.

Diabetic retinopathy

Microvascular changes consistent with diabetic retinopathy have been reported prior to and after treatment of diabetic ketoacidosis; the blood-retinal barrier does not experience the same degree of perturbation as the blood-brain barrier does, however.

See Diabetic Retinopathy for more complete information on this topic.

Hypoglycemia In patients with diabetic ketoacidosis, hypoglycemia may result from inadequate monitoring of glucose levels during insulin therapy.

Hypokalemia Hypokalemia is a complication that is precipitated by failing to rapidly address the total body potassium deficit brought out by rehydration and insulin treatment, which not only reduces acidosis but directly facilitates potassium reentry into the cell.

Consultations An endocrinologist also may be consulted to assist with management after the patient has been stabilized adequately.

Any mental status change in pediatric patients suggests the possibility of cerebral edema, and when this occurs, a pediatric endocrinologist or pediatric intensivist should be consulted as soon as possible. Psychological counseling of young children and adolescents usually is helpful.

Long-Term Monitoring Frequent blood glucose monitoring at home makes DKA less likely, as this allows them to promptly search for possible reasons for unexpectedly high blood glucose values before the condition progresses to DKA.

In a study of 127 patients with DKA who were admitted to a pediatric intensive care unit, Bradley and Tobias concluded that multiple weaknesses existed in the prehospital care of these patients.[22] These included lack of appropriate laboratory evaluation, excessive insulin dosing (both bolus doses and infusion rates), lack of fluid resuscitation, use of inappropriate fluids for resuscitation, and the use of sodium bicarbonate.

Medication Summary Regular and analog human insulins[23] are used for correction of hyperglycemia, unless bovine or pork insulin is the only available insulin. Clinical considerations in treating diabetic ketoacidosis (DKA) include the following:

Only short-acting insulin is used for correction of hyperglycemia in DKA. The optimal rate of glucose decline is 100 mg/dL/h. The blood glucose level should not be allowed to fall lower than 200 mg/dL during the first 4-5 hours of treatment. Avoid induction of hypoglycemia because it may develop rapidly during correction of ketoacidosis and may not provide sufficient warning time. Treatment of ketoacidosis should aim to correct dehydration, reverse the acidosis and ketosis, reduce plasma glucose concentration to normal, replenish electrolyte and volume losses, and identify the underlying cause.

According to the 2011 JBDS DKA guideline, patients who are already taking long-acting insulin analogues such as glargine or detemir should be maintained at their usual doses.[12, 13]

Rapid-acting insulins Class Summary Rapid-acting insulins have a rapid onset and short duration of action and are associated with less hypoglycemia than regular insulin.

View full drug information Insulin aspart (NovoLog) Insulin aspart has an onset of action of 5-15 minutes. The peak effect occurs within 30-90 minutes, and its usual duration of action is 4 hours.

View full drug information Insulin glulisine (Apidra) Insulin glulisine has an onset of action of 5-15 minutes. The peak effect occurs within 30-90 minutes, and its usual duration of action is 4 hours.

View full drug information Insulin lispro (Humalog) Insulin lispro has an onset of action of 5-15 minutes, and its usual duration of action is 4 hours.

Short-acting insulins Class Summary Insulin suppresses hepatic glucose output and enhances glucose uptake by peripheral tissues. Insulin also suppresses ketogenesis and lipolysis, stimulates proper use of glucose by the cells, and reduces blood sugar levels. Only short-acting insulin is used for correction of hyperglycemia.

View full drug information Regular insulin (Humulin R, Novolin R) Regular insulin has an onset of action of 0.5-1 hours. Its peak effect occurs within 2-4 hours, and its usual duration of action is 4-6 hours.

Electrolyte Supplement Class Summary Serum potassium levels initially are high or within the reference range in patients with DKA. This needs to be checked frequently, as values drop very rapidly with treatment. Supplements such as potassium chloride work to correct such electrolyte imbalances.

View full drug information Potassium chloride (Klor-Con, K-Dur, Kaon Cl) Potassium deficits are high in patients with diabetic ketoacidosis, even with paradoxically high K+ due to acidotic state, which shifts H+ into cells and K+ out of cells into blood. Repletion with potassium phosphate often thought unnecessary, although some recommend giving potassium phosphate to replete both of these electrolytes. Potassium replacement should be started with initial fluid replacement if potassium levels are normal or low. Monitor the potassium level every 1-2 hours initially.

Alkalinizing Agents

These agents may be used as a temporizing measure in very severe acidosis and in patients who become hemodynamically unstable because of the acidosis.

View full drug information Sodium bicarbonate (Neut) Sodium bicarbonate is only infused if decompensated acidosis starts to threaten the patient's life, especially when associated with either sepsis or lactic acidosis. If sodium bicarbonate is indicated, 100-150 mL of 1.4% concentration is infused initially. This may be repeated every half hour if necessary. Rapid and early correction of acidosis with sodium bicarbonate may worsen hypokalemia and cause paradoxical cellular acidosis.

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